台大心理系

 Asthma is a chronic inflammatory disease of the airways that is accompanied by episodes of airway constriction, shortness of breath, and nighttime symptoms. The importance of emotional processes in asthma has long been observed, but only recently asthma guidelines have acknowledged their importance as precipitants of symptoms and exacerbations. Across countries and populations, systematic surveys consistently show that approximately 15-30 % percent of patient report psychological factors as top triggers of their asthma. Affective disorders are more prevalent in asthma, but their relationship with asthma-typical nighttime symptoms is virtually unexplored. Psychological trigger reports approximately double the risk for low asthma control over and above anxiety and depression. Laboratory airway constriction to emotional stimuli is associated with patients’ reports of psychological triggers of their asthma and with bronchoconstriction to strong negative mood states in daily life. Studies of associations with heart rate variability/respiratory sinus arrhythmia (controlled for respiration) and pharmacological blockade show that these airway constrictions are vagally mediated and have a fast onset. Observational studies in daily life have documented asthma exacerbations following negative life events and heightened airway inflammatory responses in periods of stress, which may be related to underperformance of the hypothalamic-pituitary-adrenal axis in asthma. Most recently, brain imaging studies have begun to show associations of cortical and subcortical areas of asthma patients with emotion-induced bronchoconstriction and aspects of airway inflammation. There is also a growing realization that the asthmatic disease itself affects the brain through a number of pathways and mechanisms, including sleep disruption by night-time symptoms and medication use. Studies have uncovered disease-related variations in structural, functional, and chemical processes of the brain, with possible consequences for affect and cognitive function. Thus, evidence has accumulated for a bidirectional lung-brain axis, which can be compromised in asthma.